A study of molecular pathogenesis of chronic pancreatitis by using polycystic kidney rat

2014 Fiscal Year Final Research Report

• Project/Area Number: 24591010
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Nagoya University
• Principal Investigator: ISHIGURO Hiroshi 名古屋大学, 総合保健体育科学センター, 教授 (90303651)
• Co-Investigator(Kenkyū-buntansha): FURUYA Sonoko 生理学研究所・個別研究, 村上正隆, 特別協力研究員 (20096952) ; NAGAO Shizuko 藤田保健衛生大学, 疾患モデル教育研究センター, 准教授 (20183527) ; NAKAKUKI MIyuki 名古屋大学, 総合保健体育科学センター, 非常勤研究員 (30578729) ; YAMAMOTO Akiko 名古屋大学, 総合保健体育科学センター, 准教授 (60402385)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 膵管 / primary cilia / 多発性嚢胞腎症

Outline of Final Research Achievements

To clarify the role of primary cilia in the pancreatic duct, we examined the structure and function of the exocrine pancreas of polycystic kidney (PCK) rats. Pancreatic fluid secretion in vivo stimulated with a physiological dose of secretin in PCK rats was significantly smaller than that in wild-type (WT) rats. The amylase response to carbamylcholine was not different between PCK and WT rats. In isolated interlobular pancreatic duct of PCK rats, fluid secretion stimulated with the maximal concentration of secretin was significantly larger compared to WT duct. In WT ducts, a luminal application of ATP from the acinar side induced a significantly larger intracellular Ca2+ response than that applied from the duodenal side. The direction of ATP flow induced the opposite intracellular Ca2+ response to in PCK ducts. Luminal mucus was removed by luminal perfusion of N-acetylcysteine and primaly cila protruded from epithelial cells were successfully observed by electron microscope.

Free Research Field

膵臓病学